The vicious circle between mitochondrial oxidative stress and dynamic abnormality mediates triethylene glycol dimethacrylate-induced preodontoblast apoptosis

Huang, SB; X, Jin; Qh, Yu; Xr, Zhang; Bb, Zheng; Kh, Wang; Sun, Xi; Yt, Chen; Xr, Ren; Ma, JF; Wu, Guangjun; Yh, Pan

doi:10.1016/j.freeradbiomed.2019.02.013

Cited by 18 publications

(13 citation statements)

References 58 publications

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“…Mikulás et.al have found that TEGDMA inhibited Complex I in the respiratory chains of mitochondria isolated from guinea pig brain [35] . Nonetheless, our research demonstrated that TEGDMA damaged the Complex III activity of preodontoblasts, the disordered mitochondria manifested as ATP synthesis decrease and mtROS production increase [15] . Furthermore, mtROS generation is believed to be dependent on membrane potential of mitochondria.…”

Section: Discussionmentioning

confidence: 62%

“…Previous researches showed the cytotoxicity of TEGDMA to oral tissues involves in accumulating mtROS and irreversible mitochondria damage [13] [14] . Our latest study has also demonstrated that mitochondrial dysfunction was the major factors in the pre-odontoblasts apoptosis induced by TEGDMA [15] . However, the detailed mechanism, especially the signaling pathway to regulate the mitochondrial dysfunction in TEGDMA induced cell apoptosis need to be further explored.…”

Section: Introductionmentioning

confidence: 86%

“…Cells were treated with TEGDMA and other test compounds for 1 h. Then, the cells were incubated in fresh culture medium containing 2 µM MitoSOX for 30 mins. To assess the MMP, cells were co-stained with Mitogreen (100 nM) and TMRM (100 nM) for 30 min, according to our previous work [15] , Images were captured under a uorescence microscope. Excitation wavelengths were 543 nm for MitoSOX and TMRM and 488 nm for Mitogreen.…”

Section: Mitochondrial Functional Imaging Assaysmentioning

confidence: 99%

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Melatonin Protects TEGDMA induced Pre-odontoblasts Mitochondrial Apoptosis via JNK/MAPK Signaling Pathway

Yu¹,

Liu

Wang³

et al. 2021

Preprint

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Background: Resin monomer induced dental pulp injury presents a mitochondrial dysfunction related pathology. Melatonin has been regarded as a strong mitochondrial protective bioactive compound from pineal gland. However, it remains unknown whether melatonin can prevent dental pulp from resin monomer induced injury. The aim of the study is to investigate the effects of melatonin on TEGDMA, a major component in dental resin, induced mouse pre-odontoblast cell lines (mDPC6T) mitochondrial apoptosis and to verify whether JNK/MAPK signaling pathway mediate the protective effect of melatonin. Methods: We adopted a well-established TEGDMA-induced mDPC6T apoptosis model to investigate the preventive effect of melatonin by detecting cell viability, apoptosis rate, expression of apoptosis related protein, mitochondrial ROS (mtROS) production, mitochondrial membrane potential (MMP) and adenosine triphosphate (ATP) level. Inhibitors of MAPKs signaling were used to explore which pathway was participated in TEGDMA induced apoptosis. Finally, we verified the role of JNK/MAPK pathway during the protective effects of melatonin above by the agonist and antagonists of JNK.Results: Melatonin attenuated TEGDMA induced mDPC6T apoptosis via reducing mtROS production, rescuing MMP and ATP level. Meanwhile, the mitochondrial dysfunction and apoptosis was alleviated by the JNK/MAPK inhibitor SP600125 but not the other MAPKs signaling inhibitors. Furthermore, melatonin down-regulated the expression of phosphorylated-JNK, and eliminated the active effects of Anisomycin on JNK/MAPK pathway, which mimicked the effects of the SP600125.Conclusion: Our findings demonstrated that melatonin protected mDPC6T against TEGDMA induced apoptosis via JNK/MAPK signaling and maintenance of mitochondrial function, which presented a novel therapeutic strategy for prevention against resin monomer-induced dental pulp injury.

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Section: Discussionmentioning

confidence: 62%

Section: Introductionmentioning

confidence: 86%

Section: Mitochondrial Functional Imaging Assaysmentioning

confidence: 99%

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Melatonin Protects TEGDMA induced Pre-odontoblasts Mitochondrial Apoptosis via JNK/MAPK Signaling Pathway

Yu¹,

Liu

Wang³

et al. 2021

Preprint

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“…Our previous study demonstrated that oxidative stress had been associated with changes in mitochondrial dynamics in cardiac tissues ( 11 ). Only a few studies have shown that oxidative stress can change mitochondrial dynamics in mouse pre-odontoblasts ( 2 , 14 ). There has been limited research into the association between oxidative stress and the disturbance of mitochondrial dynamics in the human dental pulp.…”

Section: Introductionmentioning

confidence: 99%

The Observation of Inflammation, Oxidative Stress, Mitochondrial Dynamics, and Apoptosis in Dental Pulp following a Diagnosis of Irreversible Pulpitis

Vaseenon¹

2022

Eur Endod J

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Objective Mitochondrial dynamics play a pivotal role in maintaining the homeostasis of the dental pulp. Inflammation and oxidative stress can trigger changes in mitochondrial dynamics, leading to cell death in the dental pulp. This study aimed to investigate inflammation, oxidative stress, mitochondrial dynamic alterations, and cell death in inflamed pulpal tissues compared to healthy pulp tissues. Methods Pulpal tissues were collected (n=15 per group) from: 1) healthy people as the control and 2) people with clinically diagnosed irreversible pulpitis. Proteins indicating inflammation, oxidative stress, mitochondrial dynamics, and cell death markers were investigated by western blot analysis. A Student’s t-test was used to analyse differences between the healthy and irreversible pulpitis groups. A probability of 0.05 was used to indicate statistical significance (p<0.05). Results The expression of the proteins, tumour necrosis factor-alpha (TNF-α) and nuclear factor kappa-light-chain-enhancer, by activated B cells (NF-κB) from inflamed pulp tissues were significantly higher than those of control. Compared to controls, 4 hydroxynonenal (4HNE) and dynamin-related protein 1 (Drp1) were significantly higher, while mitofusin 2 (MFN2) and optic atrophy type 1 (OPA1) were significantly lower in inflamed pulp tissues. Bcl-2-associated X protein (Bax), cleaved caspase-3, and cytochrome c were significantly higher in inflamed pulpal tissues compared to controls. In inflamed pulpal tissues, we found a significant increase in the expression of receptor-interacting serine or threonine-protein kinase 1 (RIPK1) but not receptor-interacting serine or threonine-protein kinase 3 (RIPK3). Conclusion Irreversible pulpitis is associated with inflammation, oxidative stress, alterations in mitochondrial dynamics, and apoptosis in pulpal tissues.

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“…Increased gelatinolytic activity in "caries-affected" dentine tubules under composite restorations may facilitate TEGDMA reaching the pulp [16]. Efforts concerning TEGDMA toxicity in pulp tissue have focused on glutathione depletion, DNA damage and redox alteration [17][18][19], but the effect on MMPs, as possible contributors to both secondary caries and pulpal inflammation, is incompletely understood. The effect of different adhesives on pulp-derived and in situ dentine MMPs has been described [20][21][22][23].…”

Section: Introductionmentioning

confidence: 99%

Influence of TEGDMA monomer on MMP-2, MMP-8, and MMP-9 production and collagenase activity in pulp cells

et al. 2020

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Objectives Resin-based composites may leach monomers such as triethylene-glycol dimethacrylate (TEGDMA), which could contribute to intrapulpal inflammation. The aim of this investigation was to examine whether various concentrations of TEGDMA are able to influence dentally relevant Matrix metalloproteinase (MMP)-2, MMP-8, and MMP-9 production, total collagenase/gelatinase activity in pulp cells, and suggest possible signaling mechanisms. Materials and methods Pulp cells were cultured, followed by a 1-day exposure to sublethal TEGDMA concentrations (0.1, 0.2, and 0.75 mM). Total MMP activity was measured by an EnzCheck total collagenase/gelatinase assay, while the production of specific MMPs and the relative changes of phosphorylated, i.e., activated signaling protein levels of extracellular signal-regulated kinase (ERK)1/2, p38, c-Jun N-terminal kinase (JNK) were identified by western blot. Immunocytochemistry image data was also plotted and analyzed to see whether TEGDMA could possibly alter MMP production. Results An increase in activated MMP-2, MMP-8, and MMP-9 production as well as total collagenase activity was seen after a 24-h exposure to the abovementioned TEGDMA concentrations. Increase was most substantial at 0.1 (P = 0.002) and 0.2 mM (P = 0.0381). Concurrent pERK , p-p38, and p-JNK elevations were also detected. Conclusions Results suggest that monomers such as TEGDMA, leached from resin-based restorative materials, activate and induce the production of dentally relevant MMPs in pulp cells. Activation of ERK1/2, p38, or JNK and MMP increase may play a role in and/or can be part of a broader stress response. Clinical relevance Induction of MMP production and activity may further be components in the mechanisms of intrapulpal monomer toxicity.

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The vicious circle between mitochondrial oxidative stress and dynamic abnormality mediates triethylene glycol dimethacrylate-induced preodontoblast apoptosis

Cited by 18 publications

References 58 publications

Melatonin Protects TEGDMA induced Pre-odontoblasts Mitochondrial Apoptosis via JNK/MAPK Signaling Pathway

Melatonin Protects TEGDMA induced Pre-odontoblasts Mitochondrial Apoptosis via JNK/MAPK Signaling Pathway

The Observation of Inflammation, Oxidative Stress, Mitochondrial Dynamics, and Apoptosis in Dental Pulp following a Diagnosis of Irreversible Pulpitis

Influence of TEGDMA monomer on MMP-2, MMP-8, and MMP-9 production and collagenase activity in pulp cells

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